Acute limb ischemia can be embolic, thrombotic, or traumatic. Symptoms and signs are related to the location of the occlusion, the duration of ischemia, and the degree of development of collateral circulation. Baseline pulse examination and assessment of motor and sensory function are imperative. Characteristically, acute ischemia is described by the six Ps: pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis. Pain and paresthesias are the most common early symptoms.
The following differential points should be considered: (1) Are there manifestations of advanced occlusive arterial disease in other areas, especially the opposite extremity (bruit, absent pulses, secondary skin changes), and is there a history of intermittent claudication? These findings suggest primary arterial thrombosis. (2) Is there a history of rheumatic heart disease, atrial fibrillation, or myocardial infarction? These findings suggest embolism.
Eighty to 90 percent of arterial emboli arise from the heart. Atrial fibrillation is present in 60-70% of patients with arterial emboli and is associated with formation of thrombus in the left atrial appendage. Thrombus within a postinfarct ventricular aneurysm may also be a potential embolic source. Emboli arising from rheumatic heart disease are decreasing in incidence and now comprise less than 20% of arterial emboli. Cardiac valvular prostheses and cardiac tumors (myxomas) can also produce emboli. Noncardiac emboli arise from atherosclerotic lesions in proximal vessels, tumors, and foreign bodies. Paradoxical emboli deriving from Deep venous thrombosis in the leg can also occur.
Emboli tend to lodge at the bifurcation of major arteries, with 40% going to the aortic, femoral, or popliteal bifurcations. Thirty percent lodge in the cerebrovascular vessels, 10% in the visceral vessels, and 15% in the upper extremity vessels. Noncardiac emboli from arterial ulcerations are usually small (< 400 um), giving rise to peripheral ulceration and digital ischemia or occasionally to a systemic illness resembling vasculitis.
Heparin sodium should be given as soon as the diagnosis of acute arterial occlusion is made and continued intraoperatively to prevent distal thrombosis. Emergent embolectomy is performed by introducing a balloon catheter through a small arteriotomy. An embolus at the aortic bifurcation or in the iliac artery can often be removed under local anesthesia through unilateral or bilateral common femoral arteriotomies. Smaller balloon catheters passed distally from the femoral artery can be used to extract popliteal or tibial emboli, though these often require popliteal arteriotomy. Percutaneous catheter techniques (aspiration, mechanical thrombolysis, or thrombolytic therapy) have some reported success in treatment of peripheral embolic disease. Lifelong anticoagulation is recommended because of the high frequency of recurrent emboli. Surface or transesophageal echocardiography should be performed to exclude the possibility of atrial thrombus, valvular disease, or cardiac tumor.
Embolectomy performed more than 6 hours following onset of symptoms is often accompanied by development of a compartment syndrome. In mild cases, fasciotomy performed at the time of embolectomy can result in full functional recovery of the limb. The most common persistent major neurologic deficit is foot drop secondary to peroneal nerve ischemia. Myoglobinuria and renal failure can result from rhabdomyolysis and can be minimized with aggressive hydration, induced diuresis, and alkalinization of the urine. These measures decrease the risk of myoglobin precipitation in the renal tubules. One regimen involves initial infusion of 250 mL/h of crystalloid, half as 0.45 normal saline and the rest as D5W, with two ampules of sodium bicarbonate and 12.5 g of mannitol per liter of fluid taken if the diagnosis is delayed. Severe cases of compartment syndrome may result in anuric renal failure and systemic inflammatory response syndrome. In these patients, primary amputation may be life-saving.
Arterial embolism is associated with a 5-25% risk of limb loss and a 25-30% in-hospital mortality. Heart disease is responsible for the majority of these deaths.
In patients with atrial fibrillation, mechanical or pharmacologic cardioversion or long-term anticoagulant therapy may decrease the risk of further emboli.
If no heart disease exists, prognosis is dependent on identification and exclusion of the embolic source. Cholesterol emboli from proximal arterial aneurysm or ulceration may occlude small distal vessels, producing digital ischemia. One common scenario is “blue toes” after aortography or aortic cross-clamping for coronary artery bypass or aneurysm repair. However, atheroemboli can also produce transient ischemic attacks, acute renal insufficiency, or bowel ischemia depending on their location. Microhematuria, eosinophilia, and an elevated sedimentation rate are detectable transiently on laboratory testing. Biopsy of the infarcted tissue reveals cholesterol clefts in the small vessels under polarized light. These lesions are not treatable by embolectomy because the vessels involved are so small, and heparinization may worsen the problem by liberating more fragments from an ulcerated atherosclerotic plaque. Aortic or iliac lesions can be treated by endarterectomy, by resection and interposition graft, or by placement of a covered stent.
Acute arterial thrombosis is most commonly a complication of chronic atherosclerotic occlusive disease but can also occur as a consequence of trauma, low-flow states such as hypovolemic or cardiogenic shock, or an inflammatory arteritis. Polycythemia, dehydration, and hypercoagulable states also increase the risk of thrombosis. Generally, thrombus starts at the point of greatest stenosis and propagates distally to the next open branch point, such as a patent collateral vessel.
Nonoperative treatment is the initial approach for many patients with acute arterial thrombosis. Because thrombosis develops in the setting of chronic occlusive disease, there are usually well-developed collaterals and little arterial spasm. The extremity is able to tolerate the longer periods of ischemia required for catheter-directed thrombolysis. Instillation of alteplase (0.5-1 mg/h) directly into the thrombus through a multiside-holed catheter may allow recanalization of distal vessels that are less amenable to surgical thrombectomy. It also helps to disclose the underlying stenotic lesion, which can then be treated with angioplasty, endarterectomy, or bypass grafting. Thrombolysis is successful in 50-80% of cases, with a limb salvage rate approaching 90%.
Less commonly, arterial thrombosis follows penetrating trauma, such as arterial transection and foreign body embolization, or blunt trauma, such as posterior knee dislocation and crush injury. These patients require surgical treatment. The vessel involved may be previously undiseased, with only a few small collaterals. Thrombolysis is generally not indicated because of the more advanced state of limb ischemia on presentation and the high incidence of bleeding complications.
Limb salvage is usually possible with acute thrombosis of the iliac or superficial femoral arteries but is less likely with popliteal thrombosis because of the paucity of available collaterals. Acute thrombosis of a popliteal aneurysm is associated with a 10-25% risk of amputation.
Ouriel K: Current status of thrombolysis for peripheral arterial occlusive disease. Ann Vasc Surg 2002;16:797.
Van Cott EM et al: Laboratory evaluation of hypercoagulability with venous or arterial thrombosis. Arch Pathol Lab Med 2002;126:1281.
Revision date: July 4, 2011
Last revised: by Andrew G. Epstein, M.D.